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10.1002/cti2.1036 http://scihub22266oqcxt.onion/10.1002/cti2.1036 C6063753!6063753!30065836     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Clin+Transl+Immunology 2018 ; 7 (7): ä Nephropedia Template TP {{tp|p=30065836|t=2018. Platelets regulate leucocyte responses to Toll?like receptor stimulation |pdf=|usr=}}{{30065836}} gab.com Text Platelets regulate leucocyte responses to Toll like receptor stimulation JO: Clin Transl Immunology http://www.kidney.de/pget.php?&tw=1&pmid=30065836 #FOAvip Objectives: Platelets are important regulators of vascular thrombosis and inflammation and are known to express Toll?like receptors (TLRs). Through TLRs, platelets mediate a number of responses by interacting with leucocytes. Here, we report the extent to which platelets modulate in vitro peripheral blood mononuclear cells (PBMCs) and granulocyte responses to TLR4, TLR2/1 and TLR2/6 stimulation in healthy subjects. Methods: Peripheral blood mononuclear cells and granulocytes from 10 healthy volunteers were cultured alone or cocultured with platelets. Cultures were left unstimulated or stimulated with 1 or 100 ng mL?1 of either LPS (TLR4 agonist), Pam3CSK4 (TLR2/1 agonist) or fibroblast?stimulating lipopeptide (FSL)?1 (TLR2/6 agonist). Neutrophil activation (CD66b expression), monocyte activation (HLA?DR), granulocyte elastase production and PBMC cytokine and chemokine production were examined. Results: Platelet coculture decreased neutrophil CD66b expression in response to LPS, Pam3CSK4 and FSL?1, and modestly decreased monocyte HLA?DR expression in response to low?dose LPS. Platelets reduced granulocyte elastase secretion in response to low doses of all TLR agonists tested. In response to LPS, platelet coculture reduced IL?6, tumor necrosis factor (TNF)?? and MIP?1? production, and increased IL?10 production by PBMCs. In response to FSL?1, platelets increased IL?6, IL?10 and MIP?1? production, but reduced TNF?? production. Platelet coculture did not alter PBMC cytokine/chemokine production in response to Pam3CSK4. Conclusion: This study challenges the notion that platelets act solely in a pro?inflammatory manner. Rather, platelets are complex immunomodulators that regulate leucocyte responses to TLR stimulation in a TLR agonist?specific manner. Platelets may modulate leucocyte responses to dampen inflammation, and this platelet effect may play an important role in reducing inflammation?mediated host damage. Twit Text FOAVip Platelets regulate leucocyte responses to Toll like receptor stimulation ????Clin Transl Immunology http://www.kidney.de/pget.php?&tw=1&pmid=30065836 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30065836 #FOAvip English Wikipedia <ref>{{Cite pmid|30065836}}</ref> Platelets regulate leucocyte responses to Toll?like receptor stimulation #MMPMID30065836 Hally KE; La Flamme AC; Harding SA; Larsen PD Clin Transl Immunology 2018[]; 7 (7): ä PMID30065836show ga Objectives: Platelets are important regulators of vascular thrombosis and inflammation and are known to express Toll?like receptors (TLRs). Through TLRs, platelets mediate a number of responses by interacting with leucocytes. Here, we report the extent to which platelets modulate in vitro peripheral blood mononuclear cells (PBMCs) and granulocyte responses to TLR4, TLR2/1 and TLR2/6 stimulation in healthy subjects. Methods: Peripheral blood mononuclear cells and granulocytes from 10 healthy volunteers were cultured alone or cocultured with platelets. Cultures were left unstimulated or stimulated with 1 or 100 ng mL?1 of either LPS (TLR4 agonist), Pam3CSK4 (TLR2/1 agonist) or fibroblast?stimulating lipopeptide (FSL)?1 (TLR2/6 agonist). Neutrophil activation (CD66b expression), monocyte activation (HLA?DR), granulocyte elastase production and PBMC cytokine and chemokine production were examined. Results: Platelet coculture decreased neutrophil CD66b expression in response to LPS, Pam3CSK4 and FSL?1, and modestly decreased monocyte HLA?DR expression in response to low?dose LPS. Platelets reduced granulocyte elastase secretion in response to low doses of all TLR agonists tested. In response to LPS, platelet coculture reduced IL?6, tumor necrosis factor (TNF)?? and MIP?1? production, and increased IL?10 production by PBMCs. In response to FSL?1, platelets increased IL?6, IL?10 and MIP?1? production, but reduced TNF?? production. Platelet coculture did not alter PBMC cytokine/chemokine production in response to Pam3CSK4. Conclusion: This study challenges the notion that platelets act solely in a pro?inflammatory manner. Rather, platelets are complex immunomodulators that regulate leucocyte responses to TLR stimulation in a TLR agonist?specific manner. Platelets may modulate leucocyte responses to dampen inflammation, and this platelet effect may play an important role in reducing inflammation?mediated host damage. äPlatelets regulate leucocyte responses to Toll?like receptor stimulati(epmc).pdf DeepDyve Pubget Overpricing